108 results on '"Joan M. Carboni"'
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2. Supplementary Figures S1-S5 from IRS2 Copy Number Gain, KRAS and BRAF Mutation Status as Predictive Biomarkers for Response to the IGF-1R/IR Inhibitor BMS-754807 in Colorectal Cancer Cell Lines
3. Supplementary Figure 1, Tables 1-2 from IGFBP Ratio Confers Resistance to IGF Targeting and Correlates with Increased Invasion and Poor Outcome in Breast Tumors
4. Supplementary Tables 1-6 from BMS-754807, a small molecule inhibitor of insulin-like growth factor-1R/IR
5. Supplementary Figure 1 from Drug Efflux by Breast Cancer Resistance Protein Is a Mechanism of Resistance to the Benzimidazole Insulin-Like Growth Factor Receptor/Insulin Receptor Inhibitor, BMS-536924
6. Supplementary Figures S1-S4 from High IGF-IR Activity in Triple-Negative Breast Cancer Cell Lines and Tumorgrafts Correlates with Sensitivity to Anti–IGF-IR Therapy
7. Data from IGFBP Ratio Confers Resistance to IGF Targeting and Correlates with Increased Invasion and Poor Outcome in Breast Tumors
8. Supplementary Figure 3 from Drug Efflux by Breast Cancer Resistance Protein Is a Mechanism of Resistance to the Benzimidazole Insulin-Like Growth Factor Receptor/Insulin Receptor Inhibitor, BMS-536924
9. Supplementary Figure 2B from Drug Efflux by Breast Cancer Resistance Protein Is a Mechanism of Resistance to the Benzimidazole Insulin-Like Growth Factor Receptor/Insulin Receptor Inhibitor, BMS-536924
10. Supplementary Figure Legends from Drug Efflux by Breast Cancer Resistance Protein Is a Mechanism of Resistance to the Benzimidazole Insulin-Like Growth Factor Receptor/Insulin Receptor Inhibitor, BMS-536924
11. Supplementary Figure 1 from BMS-754807, a small molecule inhibitor of insulin-like growth factor-1R/IR
12. Data from BMS-754807, a small molecule inhibitor of insulin-like growth factor-1R/IR
13. Legends for Supplementary Figures 1-2, Tables 1-6 from BMS-754807, a small molecule inhibitor of insulin-like growth factor-1R/IR
14. Data from BMS-536924 Reverses IGF-IR-Induced Transformation of Mammary Epithelial Cells and Causes Growth Inhibition and Polarization of MCF7 Cells
15. Data from Drug Efflux by Breast Cancer Resistance Protein Is a Mechanism of Resistance to the Benzimidazole Insulin-Like Growth Factor Receptor/Insulin Receptor Inhibitor, BMS-536924
16. Supplementary Figure S1 from BMS-536924 Reverses IGF-IR-Induced Transformation of Mammary Epithelial Cells and Causes Growth Inhibition and Polarization of MCF7 Cells
17. Supplementary Figure 2 from BMS-754807, a small molecule inhibitor of insulin-like growth factor-1R/IR
18. Data from High IGF-IR Activity in Triple-Negative Breast Cancer Cell Lines and Tumorgrafts Correlates with Sensitivity to Anti–IGF-IR Therapy
19. Data from Differential Mechanisms of Acquired Resistance to Insulin-like Growth Factor-I Receptor Antibody Therapy or to a Small-Molecule Inhibitor, BMS-754807, in a Human Rhabdomyosarcoma Model
20. Supplementary Figure 1A from Dual IGF-1R/InsR Inhibitor BMS-754807 Synergizes with Hormonal Agents in Treatment of Estrogen-Dependent Breast Cancer
21. Supplementary Figures 1-8 from The Mechanisms of Differential Sensitivity to an Insulin-like Growth Factor-1 Receptor Inhibitor (BMS-536924) and Rationale for Combining with EGFR/HER2 Inhibitors
22. Supplementary Figures 1-10, Tables 1-5 from Differential Mechanisms of Acquired Resistance to Insulin-like Growth Factor-I Receptor Antibody Therapy or to a Small-Molecule Inhibitor, BMS-754807, in a Human Rhabdomyosarcoma Model
23. Supplementary Figure and Table Legends from ETV6-NTRK3–Mediated Breast Epithelial Cell Transformation Is Blocked by Targeting the IGF1R Signaling Pathway
24. Data from Insulin-Mediated Acceleration of Breast Cancer Development and Progression in a Nonobese Model of Type 2 Diabetes
25. Supplementary Figure Legends 1-3, Table 1 from Dual IGF-1R/InsR Inhibitor BMS-754807 Synergizes with Hormonal Agents in Treatment of Estrogen-Dependent Breast Cancer
26. Supplementary Microarray Data from Dual IGF-1R/InsR Inhibitor BMS-754807 Synergizes with Hormonal Agents in Treatment of Estrogen-Dependent Breast Cancer
27. Supplementary Methods from Insulin-Mediated Acceleration of Breast Cancer Development and Progression in a Nonobese Model of Type 2 Diabetes
28. Supplementary Table 1 from Expression of Insulin Receptor Isoform A and Insulin-like Growth Factor-1 Receptor in Human Acute Myelogenous Leukemia: Effect of the Dual-Receptor Inhibitor BMS-536924 In vitro
29. Supplementary Tables 1-4 from The Mechanisms of Differential Sensitivity to an Insulin-like Growth Factor-1 Receptor Inhibitor (BMS-536924) and Rationale for Combining with EGFR/HER2 Inhibitors
30. Supplementary Materials, Table 1-2, Figures 1-5 from Synthetic Lethality Screens Reveal RPS6 and MST1R as Modifiers of Insulin-like Growth Factor-1 Receptor Inhibitor Activity in Childhood Sarcomas
31. Supplementary Figure 3 from Dual IGF-1R/InsR Inhibitor BMS-754807 Synergizes with Hormonal Agents in Treatment of Estrogen-Dependent Breast Cancer
32. Supplementary Figure Legends 1-5 from Insulin-Mediated Acceleration of Breast Cancer Development and Progression in a Nonobese Model of Type 2 Diabetes
33. Supplementary Figures 1-6, Table 1 from ETV6-NTRK3–Mediated Breast Epithelial Cell Transformation Is Blocked by Targeting the IGF1R Signaling Pathway
34. Supplementary Figure 2B from Dual IGF-1R/InsR Inhibitor BMS-754807 Synergizes with Hormonal Agents in Treatment of Estrogen-Dependent Breast Cancer
35. Combined Inhibition of IGF-1R/IR and Src family kinases enhances antitumor effects in prostate cancer by decreasing activated survival pathways.
36. IRS2 Copy Number Gain, KRAS and BRAF Mutation Status as Predictive Biomarkers for Response to the IGF-1R/IR Inhibitor BMS-754807 in Colorectal Cancer Cell Lines
37. IGF1/insulin receptor kinase inhibition by BMS-536924 is better tolerated than alloxan-induced hypoinsulinemia and more effective than metformin in the treatment of experimental insulin-responsive breast cancer
38. A tripartite complex composed of ETV6-NTRK3, IRS1 and IGF1R is required for ETV6-NTRK3-mediated membrane localization and transformation
39. High IGF-IR Activity in Triple-Negative Breast Cancer Cell Lines and Tumorgrafts Correlates with Sensitivity to Anti–IGF-IR Therapy
40. Synthetic Lethality Screens Reveal RPS6 and MST1R as Modifiers of Insulin-like Growth Factor-1 Receptor Inhibitor Activity in Childhood Sarcomas
41. Differential Mechanisms of Acquired Resistance to Insulin-like Growth Factor-I Receptor Antibody Therapy or to a Small-Molecule Inhibitor, BMS-754807, in a Human Rhabdomyosarcoma Model
42. Insulin Receptor (IR) Pathway Hyperactivity in IGF-IR Null Cells and Suppression of Downstream Growth Signaling Using the Dual IGF-IR/IR Inhibitor, BMS-754807
43. Insulin-like growth factor-1 receptor (IGF-1R) kinase inhibitors: SAR of a series of 3-[6-(4-substituted-piperazin-1-yl)-4-methyl-1H-benzimidazol-2-yl]-1H-pyridine-2-one
44. BMS-536924 sensitizes human epithelial ovarian cancer cells to the PARP inhibitor, 3-aminobenzamide
45. Expression of Insulin Receptor Isoform A and Insulin-like Growth Factor-1 Receptor in Human Acute Myelogenous Leukemia: Effect of the Dual-Receptor Inhibitor BMS-536924 In vitro
46. Insulin Receptor Isoform A and Insulin-like Growth Factor II as Additional Treatment Targets in Human Osteosarcoma
47. BMS-536924 Reverses IGF-IR-Induced Transformation of Mammary Epithelial Cells and Causes Growth Inhibition and Polarization of MCF7 Cells
48. HER receptor signaling confers resistance to the insulin-like growth factor-I receptor inhibitor, BMS-536924
49. Balancing oral exposure with Cyp3A4 inhibition in benzimidazole-based IGF-IR inhibitors
50. Imidazole moiety replacements in the 3-(1H-benzo[d]imidazol-2-yl)pyridin-2(1H)-one inhibitors of insulin-like growth factor receptor-1 (IGF-1R) to improve cytochrome P450 profile
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